The N-methyl-D-aspartate (NMDA) subtype of glutamate receptor and its associated cation channel are allosterically coupled to a strychnine-insensitive glycine receptor, forming a "supramolecular complex" (reviewed in Foster and Fagg, 1987). Excessive activation of this "supramolecular complex" has been linked to various neuropsychopharmacological disorders including seizure disorders, ischemic brain damage, and other neuropathologies (Lehmann et al, 1987; Robinson and Coyle, 1987). The structural requirements for ligand binding to strychnine-insensitive glycine receptors in this "supramolecular complex" (Kishimoto et al, 1981; Marvizon et al, 1986; Galli et al, 1988; Snell et al, 1988) and their regional distribution in the central nervous system (Bristow et al, 1986) have been reported to differ remarkably from strychnine-sensitive glycine receptors. It has also been reported that there is an absolute requirement that there be present glycine for activation of NMDA receptor complexes as expressed in Xenopus oocytes (Kleckner and Dingledine, 1988).
1-Aminocyclopropanecarboxylic Acid (ACPC) has been shown to be potent and selective partial agonist of the strychnine insensitive glycine binding site of the N-methyl-D-aspartate (NMDA) receptor complex (Marvizon, 1989).